Electromechanical consequences of LAD, RCA, and LCx infarctions in a computational biventricular model

Abstract

Myocardial infarction alters both electrical activation and mechanical performance of the ventricles, with the specific location of the scar strongly influencing the resulting electromechanical behavior. Depending on whether the infarct affects the left anterior descending (LAD), right coronary artery (RCA), or left circumflex (LCx) territories, the patterns of depolarization, wall motion, and hemodynamic output differ markedly. Understanding these location-dependent effects is essential for linking scar topology to functional impairment and arrhythmogenic risk.

We developed a realistic biventricular heart model and generated scarred variants by introducing infarcts occupying 13.2% of the left ventricle (LV) in each of the three coronary territories. Simulations were performed using the CARPentry framework, which couples ionic models for both the myocardium and Purkinje conduction system with mechanical models incorporating stretch-activated channels (SACs), active tension generation, and nonlinear tissue mechanics, integrated with the CircAdapt lumped-parameter circulation model.

For the same infarction volume, the RCA scar produced a greater reduction in LV ejection fraction (LVEF) compared to the LAD scar (14.6% vs 9.9% decrease relative to the healthy case). The area exhibiting SAC-induced depolarization was also larger in the RCA case. The LCx infarction caused the most severe impairment. No stable EF was observed, and among the last six sinus beats of the 12-beat simulation, the highest LVEF reached only 32.4% (vs. 50.7% in the healthy heart). The pressure–volume loops during these beats showed clear beat to beat changes and ectopic activity.

The findings demonstrate that infarct location substantially modulates cardiac electromechanical and hemodynamic behavior. Among the investigated cases, the LAD scar had the least impact, while the LCx scar caused the strongest impairment and triggered arrhythmogenic events, highlighting the importance of regional vulnerability in post-infarction remodeling.